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Abstract

Background: Heart failure (HF) incidence and progression have been linked to increases in sympathetic tone, which in turn is associated with increased heart rate (HR). Among HF patients, greater HR variability, associated with lower HR, correlates with better left ventricular function. These findings suggest a possible link between higher HR over time and the development of HF.

Methods: HR was evaluated over time in 9024 hypertensive patients with no history of HF at baseline in the LIFE Study. Patients were treated with losartan- or atenolol-based regimens and followed with serial ECGs annually which were used to determine HR and ECG LVH by Cornell product and Sokolow-Lyon voltage criteria.

Results: During mean follow-up of 4.7±1.1 years, HF developed in 285 patients (3.2%). Compared with patients who did not develop HF, patients who developed HF had smaller decreases in HR to last ECG prior to new HF or last in-treatment ECG (−1.7±13.4 vs −5.1±12.8 bpm), whether on losartan-(0.0±14.6 vs −2.1±12.0) or atenolol-based treatment (−3.4±12.0 vs −8.0±12.9, all p<0.001). In univariate Cox analyses, higher HR on in-treatment ECGs was associated with an increased risk of new HF, with a 42% greater risk of HF for every 10 bpm higher HR (95% CI 32–54%). In an alternative analysis, persistence or development of a HR≥84 (upper quintile of baseline HR) was associated with a 166% greater risk of developing HF (95% CI 102–249%). After adjusting for losartan vs atenolol-based treatment, baseline risk factors for HF, baseline and in-treatment systolic and diastolic blood pressure and for the known predictive value of baseline and in-treatment ECG LVH and QRS duration for new HF, higher in-treatment HR in time-varying multivariable Cox models remained strongly predictive of new HF, with a 45% increased adjusted risk for every 10 bpm higher HR (95% CI 34–57%) or a 159% increased risk of HF in patients with persistence or development of a HR≥84 (95% CI 88 to 257%, both p<0.001).